VIP also inhibited TNF-α and NO production in mouse primary microglia stimulated with Aβ42 + low dose IFN-γ, promoted microglial phagocytosis of Aβ1–42 through a PKC-dependent mechanism, and reduced Aβ deposits in the hippocampus of transgenic PS1/APP mice, a model of AD [138], suggesting a protective role for VIP in AD through modulation of microglial function. The gene discussed is PRRT2; the disease is Alzheimer disease.